Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.6K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.6K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.1K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.1K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.7K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.7K
Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

2.0K
Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
2.0K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

5.8K
DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
5.8K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Virome-wide ubiquitin ligase discovery reveals diverse mechanisms of immune evasion.

Science (New York, N.Y.)·2026
Same author

Degron-independent recruitment of KAT2A expands the target space of CRBN molecular glues.

Science (New York, N.Y.)·2026
Same author

A Type II CDK6 Degrader Enables Cellular Targeting beyond the Limits of Type II Inhibition.

Journal of the American Chemical Society·2026
Same author

Mitochondrial integrated stress response activation creates a therapeutic vulnerability to MCL-1 inhibition in acute myeloid leukemia.

Cell death & disease·2026
Same author

Author Correction: cBAF complex components and MYC cooperate early in CD8<sup>+</sup> T cell fate.

Nature·2026
Same author

ABL kinase-dependent phosphorylation of SH proteins promotes their direct interaction with CRK family SH2 domains.

FEBS letters·2026

Related Experiment Video

Updated: Jun 29, 2025

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

8.3K

Targeting DCAF5 suppresses SMARCB1-mutant cancer by stabilizing SWI/SNF.

Sandi Radko-Juettner1,2, Hong Yue3,4, Jacquelyn A Myers1

  • 1Division of Molecular Oncology, Department of Oncology, St Jude Children's Research Hospital, Memphis, TN, USA.

Nature
|March 28, 2024
PubMed
Summary

Loss of SMARCB1 tumor suppressor function in cancers is not directly caused by the mutation but by DCAF5 degrading SWI/SNF complexes. Targeting DCAF5 can reverse cancer states by restoring SWI/SNF function.

More Related Videos

Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures
07:48

Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures

Published on: December 26, 2016

11.3K
CD Spectroscopy to Study DNA-Protein Interactions
06:48

CD Spectroscopy to Study DNA-Protein Interactions

Published on: February 10, 2022

6.7K

Related Experiment Videos

Last Updated: Jun 29, 2025

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

8.3K
Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures
07:48

Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures

Published on: December 26, 2016

11.3K
CD Spectroscopy to Study DNA-Protein Interactions
06:48

CD Spectroscopy to Study DNA-Protein Interactions

Published on: February 10, 2022

6.7K

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Loss of tumor suppressor function, unlike oncogene activation, presents a therapeutic challenge as the target protein is absent.
  • SMARCB1 (SWI/SNF subunit)-mutant cancers are lethal malignancies driven by the inactivation of these chromatin-remodeling complexes.

Purpose of the Study:

  • To investigate the mechanistic consequences of SMARCB1 mutations in cancer.
  • To identify therapeutic vulnerabilities in SMARCB1-mutant cancers.

Main Methods:

  • Utilized 14 SMARCB1-mutant cell lines in a near genome-wide CRISPR screen.
  • Investigated the role of DDB1-CUL4-associated factor 5 (DCAF5) in cancer cell survival and SWI/SNF complex stability.

Main Results:

  • Identified DCAF5 as essential for the survival of SMARCB1-mutant cancers.
  • Demonstrated that DCAF5 degrades incompletely assembled SWI/SNF complexes when SMARCB1 is absent.
  • Showed that DCAF5 depletion rescues SMARCB1-deficient SWI/SNF complexes, restoring gene expression and reversing the cancer phenotype in vitro and in vivo.

Conclusions:

  • Cancer in this context arises from DCAF5-mediated degradation of SWI/SNF complexes, not solely from SMARCB1 loss.
  • Therapeutic targeting of ubiquitin-mediated quality-control factors like DCAF5 offers a potential strategy to reverse malignancies driven by disrupted tumor suppressor complexes.